Exam review GIT and Liver, Gall bladder. Liver Hepatitis Circulatory diseases.
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Transcript of Exam review GIT and Liver, Gall bladder. Liver Hepatitis Circulatory diseases.
Exam review
GIT and Liver, Gall bladder
LiverHepatitis
Circulatory diseases
Hepatitis
Hepatitis A infection (infectious hepatitis) : RNA virus
Spread: Fecal-oral route. C/F: Never develop a carrier, chronic state , Hepatocellular carcinoma.
C/F: Mild disease, quick recovery, Acute disease: Positive for IgM antibody to hepatitis A virus (antigen).
Incidence: Sporadic outbreaks in restaurants.In places with poor hygiene. Common in childrenAdults are often seropositive
Hepatitis B infection (DNA virus)
Spread: Parenterally and by intimate contact through mucosal surfaces.
Vertical transmission is common.
Carrier state is common, Less chance of Chronic hepatitis, cirrhosis. Increased chance of Developing Hepatocellular carcinoma.Carrier: Positive HBsAg even after 6 months, with normal health but can transmit infection.
Interpretation of HBV serology
Acute phase Carrier phase Chronic
HBsAg + IgM Anti-HBs.
HBsAg +> 6 months
No surface antigen*
HBcAg + IgM Anti-HBc
IgGAnti-HBc > 6
months
IgGAnti-HBc > 6 months
DNA polymerase/ HBV DNA
HBV DNA HBV DNA
Hepatitis C infection (non-A, non-B hepatitis)RNA virus
Spread : Parenterally and via contact-associated mechanisms.Vertical transmission is NOT common. C/F : More chance of Chronic hepatitis cirrhosis and Hepatocellular carcinoma.Acute disease: Positive for IgM antibody to hepatitis C virus antigen.Chronic disease: Positive for IgG antibody to hepatitis C virus (antigen). Fatty change seen.Incidence: It is seen most commonly in the homosexual community, intravenous drug users, and patients who have received multiple blood transfusions.
Delta virus infectionRNA virus that is replication defective : cause
infection when encapsulated by HBsAgCo-infection : Positive for IgM antibody to hepatitis D virus antigen and IgM antibody to HBc antigen.Super infection: Positive for IgM antibody to hepatitis D virus antigen and HBsAg.Incidence: common in drug addict and hemophiliacClinical features: Fulminant hepatitis common with this infection, cirrhosis.
Acute HepatitisLiver cell swelling, feathery degeneration
Ground glass Hepatocytes and sanded nuclei and apoptosis (HBV).
Chronic hepatitis
Symptomatic, biochemical and/or serologicalevidence of relapsing hepatic disease for more than 6 months.Etiology: HCV ( commonest )A. General features
A. Bridging necrosis and fibrosisB. Lymphoid aggregatesC. Piecemeal necrosis= interface hepatitis
Circulatory disorders of liver
These are the disease due to circulatory disturbances
Disturbance of circulation within the liver: Cirrhosis, sinusoidal dilatation, veno occlusive disease.
Disturbance of circulation Out side the liver : Shock, RHF, hepatic artery thrombosis (cause infarct), portal vein thrombosis, hepatic vein thrombosis.
Disease
• Sinusoidal dilation (aka)= Peliosis hepatis– Etiology : Anabolic steroid , danazol, OC
pill – Peliotic lesions usually disappear after
cessation of drug treatment. • Nutmeg liver/ centrilobular necrosis/
cardiac cirrhosis– Etiology : Right sided heart failure/shock
Nutmeg liver and centrilobular necrosis
Budd-Chiari syndromeDef: acute thrombotic occlusion of the hepatic vein.Etiology;
1. Polycythemia Vera2. Myeloproliferative disorder (CML)3. Use of OC pill, HCC. 4. Deficiencies in antithrombin, protein S, or
protein C, or mutations of factor V Clinical: Tender hepatomegaly, some features of PHT,
liver enzyme elevation.
Diagnostic procedure: venogram
Veno occlusive diseases (VOD)
Etiology : Immediate week after bone marrow transplantation with immunosuppressant therapy.
Pathogenesis :Fibrosis of Small hepatic vein radicles.
Clinical:tender hepatomegaly, ascites, weight gain, and jaundice
Liver infarct
• Cause:– thrombosis or compression of an intrahepatic
branch of the hepatic artery by embolism, neoplasia,sepsis.
Portal Vein Obstruction and Thrombosis
• Insidious and well tolerated • Morphology: Well demarcated area of red-
blue discoloration (infarct of Zahn), no necrosis only atrophy.
• Ascites and other manifestations of portal hypertension
Drug and toxin induces liver disease
Type of Hepatobiliary damage
Drug or toxin
Micro vesicular fatty change
Tetracycline, ethanol
Macro vesicular fatty change
Ethanol, Methotrexate and diabetes mellitus
Centrilobular necrosis Acetaminophen, halothane.
Thank you
• Please contact me if you have ant question.